Headache and Subarachnoid Hemorrhage



Headache and Subarachnoid Hemorrhage
Headache and
Subarachnoid Hemorrhage
Carly Thompson
February 19, 2009
See Rob Halls’ presentation at the end of Carly’s
Approach to headache in the ED
 Migraine
– Focus on dx, tx
Subarachnoid Hemorrhage
 Other causes of serious headache
Headache Epidemiology
4% of ED visits
 Primary Headaches
– Migraine
– Tension-Type
– Cluster
– All others!
– 1% of headaches are SAH!
Headache: Historical Features
Occult Trauma
Signs of abuse/neglect
Sudden Onset
Maximal soon after
Different than previous
Neck stiffness
Immune compromise
Head/neck infection
Jaw claudication
Temporal tenderness
Visual symptoms
Hx of malignancy
New onset >50yrs
Worse in am, head
Neuro signs
Bilateral neuro findings
Hypercoaguable state
Recent sinusitis
CO Toxicity
Worse in am
Others affected
Name 5 high risk historical features for
Subarachnoid Hemorrhage.
High Risk Features for SAH
First or worst headache of my life
Altered mental status / Seizure
Headache with exertion / intercourse
History of exercise
Location of pain: occipitonuchal
– PPV occipitonuchal headache for intracranial
pathology is 16%
Family history of SAH
– Up to 4x increased risk in 1st and 2nd degree relatives!
What is your differential for thunderclap
headache? Name 3 (other than SAH).
Thunderclap = sudden-onset, severe
Thunderclap Headache:
Differential Diagnosis
 Carotid or vertebral artery dissections
 Venous sinus thrombosis
 Pituitary apoplexy
 Hypertensive emergencies
 Cluster headache
 Cerebellar CVA
High Risk Examination Findings
Vital signs: htn, fever
Decreased, altered, fluctuating LOC
 Focal neurologic sign
 Meningismus
 Toxic appearance
 Opthamalogic findings: papilledema, subhyaloid
hemorrhage, retinal hemorrhages, decreased vision,
ciliary flush, sluggish pupillary light response
 Trauma
 Temporal artery findings
 Carotid bruit
 Nausea and vomiting: Increased ICP, hemorrhage, ANAG
 Nasal discharge with sinus tenderness: sinusitis
What is a subhyaloid hemorrhage and
when do you see it?
Subhyaloid Hemorrhage
Gravity-dependent venous
hemorrhage between
retina and vitreous
membrane, convex at
bottom, and flat at top
when sitting
Highly suggestive of SAH:
11-33% of SAH cases
Terson’s syndrome – rapid
increase in ICP assoc. with
hemorrhage – worse
Low Risk Patient
No change in headache pattern
 No new concerning historical features
 No focal neurologic symptoms or findings
No imaging indicated!
 Meta-analysis:
– 2.4% of those with normal neuro exam have
neurologic abnormalities on CT
– 0.4% of those with typical migraine symptoms
Which subsets of patients with headache
require neuroimaging in the ED?
– Name 3 groups.
Neuroimaging Indications
ACEP Clinical Policy (Ann Emerg Med 2008)
 Level B
(1) Headache and new abnormal neuro findings
 PPV 39% for intracranial pathology
 LR 3.0
(2) Sudden-onset severe headache
 10-15% have serious pathology, often SAH
(3) HIV patients with new headache
 Headache – 35% had mass lesion
 Neurologic complaint – 24% focal lesion
 1 or more of predicted all focal lesions in a series of patients:
– New seizure
– Depressed / altered LOC
– Headache different or > 3 days
Level C Evidence
 Age >50 with new headache but normal
exam, should be considered for urgent
 OR 3.3 of pathologic diagnosis
Other worrisome features that increase
probability of positive findings, but no
clear recommendations:
– Occipital location
– Worsening with Valsalva
– Headache waking from sleep
– Associated syncope
– Nausea or sensory distortion
Headache in Pregnancy
 Most headaches are benign
 CVA – risk increases 3-13x
 SAH – 20/100,000 deliveries
 Migraines: less common
– 60-70%have improvement in migraines during
Conclusion: Insufficient data to drive
recommendations for imaging.
Can response to therapy be used as a
diagnostic tool?
Response to Therapy
Level C
 No!!! Pain response should not be used.
 ? Common pathway for pain regardless of
 No RCT to support or refute this.
 Class III Evidence: Case reports, case series,
showing resolution or improvement in pain with
analgesics in SAH, meningitis, CO-induced
headache, cerebral venous sinus thrombosis,
dissection, etc.
What are the diagnostic criteria for
Migraine: Diagnosis
Recurrent headache disorder – IHS Criteria
– Headache lasts 2-72 hours
– At least 2 of:
Moderate to Severe
Aggravation by routine activity
– At least 1 of:
 Photophobia or Phonophobia
 Nausea and/or vomiting
– At least 5 attacks
– Hx, physical and neurologic exam do not suggest
other organic disease
Migraine: Diagnosis
Migraine without Aura
 Migraine with Aura:
– Aura reversible focal neurologic symptoms
that usually develop over 5-20 min and last
<60 min, headache begins during aura or
within 60 minutes
– Visual positive / negative features
– Sensory positive / negative features
– Dysphasic speech
True or False?
 Migraines can be associated with
autonomic and sinus symptoms
– i.e. nasal congestion, rhinorrhea, tearing,
colour and temperature change, changes in
pupil size
Which of the following are associated with
– Family history of migraine
– Motion sickness
– Obesity
Associated Factors
Family history and motion sickness are risk
factors for developing migraine
 Obesity is associated with increased
frequency and severity of migraines
Migraine: Treatment
US Headache Group:
 Educate pts about condition and tx; encourage active
participation in management
 Use migraine specific agents in pts with severe migraine,
and those who respond poorly to NSAIDs or combination
 Use non-oral route for pts with sig N/V
 Consider self-administered rescue meds for pts with
severe migraine
 Guard against medication overuse headaches by using
prophylactic medication in pts with frequent headaches
List 5 treatment options for migraine in
the emergency department.
Treatment Options
Analgesics: NSAIDs, acetaminophen
Serotonin Agonists
– Ergotamine
– DHE (Dihydroergotamine)
– Triptans
Dopamine Antagonists
– Chlorpromazine
– Prochlorperazine
– Metoclopramide
Steroids: Dexamethasone
Mild Analgesics in Migraine
Some pts can get optimal response with mild
analgesics (NSAIDs, acetaminophen)
 Not advisable >10x /month
 RCTs: Acetaminophen, ibuprofen, naproxen,
diclofenac, ASA, acetaminophen + ASA +
 Indomethacin: limited data, some specific
migraine types are responsive to indomethacin
for abortive therapy, benefit: suppository form
Specific tx: 5-HT 1b/d agonist ->inhibit
dural nociception
 Advantage: multiple preparations
– SC, IN, PO
RCT and systematic reviews: all triptans
have been shown effective in acute
 Pts who don’t respond to one may
respond to another
So, why don’t we commonly use triptans
in the ED?
Limitations of Triptans
More effective if used early!
– Development of central sensitization
– Patients with pregnancy, uncontrolled htn, ischemic
heart disease, peripheral vascular disease,
Prinzmetal’s angina, ischemic CVA, familial hemiplegic
migraine, basilar migraine
– 24 hours of other 5-HT agonist (ergots), MAOIs with
some triptans
– Severe liver impairment
Interactions: P450 cytochrome
Advisory July 2006 – concomitant use with
SSRIs or SNRIs increases risk of serotonin
syndrome; advise discussion of benefit vs risk
Ergots: Ergotamine
– 5HT 1b/d receptor agonist
– Alone failed to show efficacy
Side effects:
– Nausea, vomiting
– Vascular occlusion and rebound headaches
– Long-term: Associated with CAD
Avoid in pts with CAD, PVD, htn, hepatic and renal
disease and those with prolonged aura
European Consensus Panel:
 Treatment of choice in few pts due to issues of efficacy
and side effects
Ergots: Dihydroergotamine
Fewer side effects: no dependence or rebound
 Advantage: IV, IM, SC, IN use
 Contraindications:
– Htn, CAD, PVD, Prinzmetal’s, MAOIs, sepsis, severe
hepatic or renal dysfunction, high dose ASA tx,
– Hemiplegic or basilar migraine
– Within 24 hours of triptan or other serotonin agonists
– CYP3A4 inhibitors: some macrolides, antifungals,
protease inhibitors
How does DHE compare to the triptans for
– More effective?
– Same?
– Less effective?
DHE: Efficacy
vs Placebo:
– Proven by systematic review / RCTs,
especially when given with anti-emetic
vs Triptan:
– Less effective on most measures compared
head-to-head with sumatriptan
vs Dopamine Antagonist:
– Less effective than chlorpromazine on some
Dopamine Antagonists
– Antiemetic
– IV metoclopramide
– IV or IM chlorpromazine and prochlorperazine
Largactil / Thorazine
Chlorpromazine 5-15mg IV or 0.1mg/kg IV
 RCT vs Placebo (Bigal 2002 J Emerg Med):
– Significant improvement in scores of pain, nausea,
vomiting, photo/phonophobia at 60 min
– NNT 2
Side effects:
– Hypotension / Postural hypotension (18%)
 May be exacerbated by opioids, pre-tx with fluid bolus
 Alpha-antagonist
– Drowsiness
– Pregnancy: Class C
Stemetil, Compazine
Prochlorperazine 10mg IV
 Side effects:
Dystonic Reactions
Cardiac arrhythmias
Pregnancy Class C: Isolated reports of congenital
anomalies, jaundice, EPS, hyper/hyporeflexia – if
occasional low-dose suggested to be safe
FDA Alert (June 2008): Association with
increased mortality when used for treating
dementia-related psychosis
How does prochlorperazine compare to
Proclorperazine vs Metoclopramide
RCT: Coppola (1995) Annals of Emerg Med
– > 50% relief
Stematil 82%
Maxeran 48% Placebo 29%
RCT: Jones (1996) Am J of Emerg Med
– Partial or complete relief
Stematil 67% Maxeran 34% Placebo 16%
Metoclopramide: Maxeran, Reglan
Maxeran 10mg IV
 Efficacy:
– Meta-analysis Colman (2004) BMJ
 Generally poor studies
 OR 2.84 for reduction of pain in headache
 Less effective than chlorpromazine and prochlorperazine in relieving
pain, but not always statistically significant
 1 Trial: No difference between aggressive metoclopramide (20mg
IV q30 min up to 4x with diphenhydramine 25mg IV q1 hour up to
2x) vs sumatriptan 6mg SC
– Pregnancy Class B
– Can be combined with DHE, other analgesics
Side Effects:
– Drowsiness
– Dystonic reactions: <1-25%, increased risk in young males
Other Options?
Some pts will not respond to routine treatment.
 Consider wait-times, location (ED vs clinic)
 Treat aggressively.
 Do not use following meds on a chronic basis
due to habit-forming nature and rebound
– Benzos
– Opioids
– Barbiturates
How can you prevent migraine
Parenteral Dexamethasone
Colman I et al. (2008) BMJ
 Meta-analysis of 7 RCTs.
– Dexamethasone 10-25mg IV or IM vs placebo
– Similar acute pain reduction
– Recurrence rates at 72 hours RR 0.74 (0.60.9)
– NNT 9
– Similar side effect profile
Can you name the complications of a
Migraine: Complications
Status migrainosus
 Chronic migraine
 Persistent aura without infarction
 Migrainous infarction
 Migraine-triggered seizure
Migraine Tx in the ED
Fluid bolus: NS 1L bolus IV
NSAID: If used <10x/month
– Nausea / vomiting: consider PR indomethacin
– PO: acetaminophen vs ibuprofen
Dopamine antagonist:
– Stemetil 10mg IV
– Maxeran 10mg IV (Pregnancy)
– Morphine 2-5mg IV prn
DHE / Triptan:
– If early presentation, contraindications to others
– Rizatriptan, eletriptan, almotriptan
– Sumatriptan: IN, SC or Zolmitriptan: IN, PO
Subarachnoid Hemorrhage
 SAH 1% of all headaches in ED
 10% of hemorrhagic strokes
 10% of “worst headache ever”
Prevalence: 3-25 / 100,000
Mean age: 55 (Range 20-60)
Reported in pediatrics
Miss Rate?
 Variable 5-50% (30% average)
 Acceptable miss rate: 0%!
Can you name 3 causes of SAH?
Causes of SAH
Causes of SAH:
– Trauma
– Saccular Aneurysms
– Non aneurysmal: Perimesencephalic (?venous
– AVMs / Fistulae
– Illicit drug use: cocaine, amphetamines
– Arterial dissections
Can you name 3 risk factors for formation
of aneurysms?
Etiology of Aneurysms
– Familial intracranial aneurysms (dominant)
– Genetic condition: Ehlers-Danlos, Marfan’s, PCKD
– Coarctation
Traumatic: skull #, penetration, post-op, hemodynamic damage
Infectious: syphilis, mycotic
Inflammatory: vasculitis
Degenerative: atherosclerotic
Hypertension is NOT a major factor for aneurysm
How many people have aneurysms?
Aneurysms in the Public
Prevalence of saccular aneurysms
– 5% at autopsy
– 20-30% have multiple aneurysms
Can you name 3 risk factors for rupture?
Risk Factors for Rupture of
– Dose-dependent, esp. women, disappears soon after quitting, RR 2.2
– RR 2.5, OR 2.6
– Moderate to heavy consumption RR 2.1, OR 1.5
Family History
– OR 4.0
– Autosomal dominant / recessive / multifactorial / anticipation
– Elastin gene, Platelet adhesive glycoprotein
– Appetite suppressants, cold remedies, case-control study – risk factor in
Estrogen deficiency
– Premenopausal women and reduced risk compared to age-matched
postmenopausal women (OR 0.24), HRT (OR 0.47)
Physical Exertion
– Orgasm, moderate exertion OR 2.7
What proportion of patients with SAH from
aneurysm have a sentinel bleed?
Sentinel Headache
30-50% of patients have a sentinel
headache that precedes SAH by 6-20 days
Clinical Features
Abrupt onset, severe headache “thunderclap”
Lateralized 30%
At night 30% (During day / activity 60%)
Onset associated with brief LOC, seizure,
nausea, vomiting
Meningismus / Aseptic meningitis
Normal neurologic findings at presentation 50%
What is the mortality of SAH?
Average: 51%
 10% prior to reaching hospital
 25% within 24 hours of onset
 45% within 30 days
What are the complications of SAH?
– Name 4.
Vasospasm and delayed cerebral ischemia
Hydrocephalus (acute / chronic)
Increased ICP
Hypothalamic dysfunction and pituitary insufficiency
Cardiac abnormalities
– Ventricular wall motion abnormalities
– Elevated BNP
Pitfalls in Diagnosis
Wasn’t the worst headache of their life!
 Neurologic exam was normal!
– 50% have normal neurologic exam!
Pain improved with treatment
– Remember: SAH CAN improve with treatment!
CT head was negative
 RBCs decreased from tubes 1-3 /
Misinterpretation of LP
 No LP done
CT Head: Limitations
Technical ability of CT scanners to identify
small hemorrhage / artifact / bone
 Protocol and age of scanner – thin slices
 Expertise of reader
 Anemia Hb<100 – blood appears isodense
 Time: decay in sensitivity
 Inability to diagnose other causes of
headache: meningitis, etc.
How sensitive is CT scan at day 1 for SAH?
 How sensitive is CT scan at day 7 for SAH?
CT Scan: Sensitivity
As blood is diluted and degraded flowing
through SA space -> decreased sensitivity
– BMJ (2006)
 <12 Hrs
 24 hrs
 >7 days
– Memory aide:
 Day
 Day
 Day
 Day
Why do you do a CT then if ruling out
CT Scan for SAH: Advantages
Traumatic LP:
– 13% may be traumatic (>400 RBCs)
LP Limitations:
– Cerebral venous thrombosis
– Unruptured aneurysm
– Arterial dissection
– Pituitary apoplexy
Does an LP need to be routinely
performed on ED patients to rule out SAH
if normal noncontrast CT head?
– Why?
Lumbar Puncture
ACEP (2008) Level B Evidence.
 Lumbar puncture should be performed to
rule out SAH.
 Rates of SAH confirmed by LP after
normal CT 2.5-3.5%
What 3 features do you see on LP in SAH?
Lumbar Puncture in SAH
(1) Elevated opening pressure
 (2) Elevated RBC count
 (3) Xanthochromia
Opening Pressure
 6-20cmH20 is normal in adults and children
 25cmH20 may be normal in obese pts
 Helpful to distinguish SAH from traumatic tap
 2/3 of SAH may have elevated opening pressure
 Other diagnoses: spontaneous intracranial
hypotension, benign intracranial hypertension,
cerebral venous sinus thrombosis
Does clearing of blood (i.e. declining RBC
count from tubes 1->4) rule out SAH?
Elevated Red Blood Cell Count
Clearing of blood is unreliable.
 There is no cutoff which has been shown
to reliably exclude SAH.
 However, if tap done late >12 hours, and
absence of xanthochromia, but presence
of RBC = negative tap.
 No way to tell traumatic tap vs SAH if
early <12 hours tap.
What is xanthochromia?
 When does it appear? How long does it
Yellow colour caused by bilirubin and
oxyhemoglobin due to lysis of RBCs
OxyHb -> Heme oxidase enzyme -> Bilirubin
Process may take 6-12 hours
 Onset: Blood in CSF for at least 2 hours
 Peak: 48 hours
 Duration: Up to 2-4 weeks
Name 2 methods for analyzing your
sample tubes for xanthochromia.
 Which is more sensitive?
Xanthochromia: Analysis
 Spin CSF, run through spectrophotometer, look for
oxyHb or bilirubin peak at 410nm and 460nm
 Most sensitive
 Low-moderate specificity
 Not always available
Visual Analysis
 Spin CSF, compare to identical test tube with equal
volume tap water against white background
 Calgary Health Region’s method
 Less sensitive, but may be >95% if >12 hours after SAH
Name 3 false positives for xanthochromia.
(Xanthochromia but no SAH!)
Xanthochromia: False Positives
 Rifampin
 Previous traumatic tap
 Traumatic tap isn’t analyzed quickly ->
 Chronic spinal cord abnormalities
Which patients can safely undergo LP
without neuroimaging?
LP Before CT?
ACEP (2008). Level C Evidence.
 Adults patients with headache and signs of
elevated ICP should have neuroimaging before
– Papilledema, absent venous pulsations of fundoscopy,
altered LOC, focal neuro deficits, signs of meningeal
In the absence of clinical findings suggestive of
increased ICP, LP can be performed without
obtaining neuroimaging.
In a patient with sudden-onset, severe
headache who has negative findings (both
CT head and LP) is there a need for
further emergent imaging?
Further Investigation
ACEP (2008). Level B Evidence.
 Patients with sudden-onset, severe headache
with negative CT head, normal opening
pressure, negative findings on CSF analysis, do
NOT need emergent angiography, and can be
discharged with follow-up recommended.
Note: Consider other causes of sudden-onset,
severe headache like pituitary apoplexy, cerebral
venous sinus thrombosis, arterial dissections,
cerebellar stroke . . . Further imaging may be
indicated to rule out these causes.
Further Investigation
Perry et al. (2008) Annals of Emerg Med.
– 2 Canadian EDs, 592 patients
– CT and LP to rule out SAH (10.3% had SAH)
 CT neg
 No xanthochromia by visual inspection
 RBCs in final tube <5 x 106RBC/L
– Others followed 6-36 months
– Rate of subsequent SAH: 0%
– Rate of subsequent aneurysm: 1 / 592 required
surgery, but “did not contribute to initial presentation”
Thank You!
Can you name 3 causes of headache that
might be associated with exertion?
Exertional Headache
– Pts with SAH more likely to have participated in exertion that
day, compared to previous OR 2.7
Carotid or Vertebral Artery Dissection
Primary Exertional Headache
– Bilateral pulsatile pain during or after exercise, lasts 5min – 48
hours, not usually assoc. with N/V
– Rule out: SAH, angina, vascular abnormalities, pheo
– Tx: indomethacin, propranolol, naproxen
Primary Headache Associated with Sexual Activity
Preorgasmic: usually secondary to muscle tension
Orgasmic: associated with CVA / dissection and SAH
Prevention: indomethacin, B-blockers, propranolol
Acute tx: triptans
Can you describe the most common
headache symptoms in brain tumour?
Brain Tumour
50% have headaches
– Tension-type (77%)
– Migraine (9%)
Typical headache:
– Bilateral, worse ipsilaterally, bending over (32%),
nausea and vomiting (40%), worse with Valsalva
Classic “early morning headache” – uncommon!
 Reliable findings:
– Nausea, vomiting, worsening with change in position,
abnormal neurologic exam, significant change in
headache pattern
Triptans: Comparison
Few trials comparing triptans head to
 Rizatriptan (Maxalt), eletriptan (Relpax),
almotriptan (Axert) had highest likelihood
of success
 Sumatriptan was recently released with
fast dissolving tabs
– Sumatriptan (Imitrex): SC, IN, PO
– Zolmitriptan (Zomig): IN, PO
Emergent Diagnoses
Core Rounds Feb19,2009
Rob Hall MD, FRCPC
41yo female PMHx DM1 on insulin
 Mild headache and Numbness right arm/mouth and
weakness left grip, subacute, 1 week
 No fever or illicit drug use
 OCP started 2 weeks ago
 No hx seizures, no trauma
 Waiting in ED bed, GTC 1 min sz, chemstrip normal,
ativan 2mg iv, post ictal and combative after, no
focal findings after sz
 Investigations?
 Thoughts on dx?
CT head (plain)
Cerebral Vein Thrombosis
“DVT of the BRAIN”
Venous clot then infarct and/or bleed at grey-white
Transverse sinus most common location, often
multiple sinuses
Clinical Presentations
– Often not typical arterial distribution
– Can be basically any description of
headache (thunderclap uncommon)
Risk Factors for CVT
(present in 85%)
Head and neck infections
 Hypercoagulable states
Hypercoag syndrome: lupus AC, protein C def, etc
Hematologic disorders: leukemias, polycythemia, thrombocytosis, sickle cell
Vasculitis: SLE, GCA, wegener’s, Bechet’s, etc
Exam findings
Highly variable
Three clues
– Head infection + Neuro symptoms
– Papilledema (? Sensitivitiy)
– Stroke findings in non-arterial distribution
LP will show elevated opening pressure without other cause
CT head (plain) findings
Sensitivity 60-70% (30-40% normal)
 Delta sign = dense triangle from hyperacute
thrombosed superior saggital sinus
 Cord sign = thrombosed cortical vein
 Venous infarcts with secondary hemorrhage in
non-arterial distribution
– HTN bleeds: thalamus, IC, CB, pons
– Venous infarct bleeds: bilateral at grey-white junction
CT head
Definitive Diagnosis
CT venography (preferred)
 MR venography
– Hypointense signal of acute thrombus mimics
normal flow. RadioGraphics 2006;26:S5-18.
Angiography (not used anymore)
CT Venography
CVT and Carotid/vert
Which is better CT or MR?
“I think that most radiologists reading these
studies would say that both CTV and CTA
have a higher sensitivity due to CT's inherent
spatial resolution advantage which is very
good on our latest multidetector
scanners. CT is our favoured study where
there is concern for venous sinus thrombosis
and carotid/vertebral dissection. The
research will catch up.”
ED Management
Dilantin if seized
 Manage elevated ICP
 Heparin
– Majority of evidence shows improvement trends (no
major large RCT showing statistically conclusive
– Shown to be safe even with hemorrhages!
– Cochrane review 2001
 RR death 0.33 (95%CI .08-1.2)
 RR death or disability 0.46 (0.16-1.3)
Further Management
Optic nerve fenestrations
 Acetazolamide
 Case reports of lytics
 LP/VP shunts
 Hemicraniectomy for severe ICP problems
Is Idiopathic Intracranial
HTN and CVT a spectrum
of disease?
IIHTN -------------------------> CVT
Idiopathic Intracranial HTN
Old terms = Pseudotumor cerebri,
Benign IHTN, meningitis Cerosa
 Diagnostic criteria for IIHTN requires
imaging to rule out CVT
Idiopathic Intracranial HTN
Opening pressure > 20 cm H20 (usu 25-45)
– Headache MUCH better after LP!
Signs/symptoms of increased ICP
No focal signs (except 6th palsy)
No mass lesion
No hydrocephalus
Normal CSF values
CTV/MRV to exclude CVT
Idiopathic Intracranial HTN
Main ED PEARL is to consider the
diagnosis and do an LP
– Obese, female, OCP
– Hypercoag states
– Subacute, unexplained headaches, return
visits, normal imaging
– Visual symptoms: blurry vision, diplopia
Carotid and Vertebral
2% of ischemic strokes overall but 20% of
ischemic CVA < 45yo
– Think of in young patient
Pathology the same with major vs minor
– May be VERY minor (yoga, cough, stretching,
– Unknown if “spontaneous” really occur
Carotid and Vertebral
Headache + Neck pain, unilateral + neuro
 Dx - CTA, MRA, angio
 CTA preffered
Giant Cell (Temporal) Arteritis:
the basics
Older person
Subacute headache
Systemic symptoms
Jaw claudication
Association with PMR
Risk of vision loss
Elevated ESR
Diagnose by temporal artery biopsy
Treat with steriods
Giant Cell Arteritis: some pearls
Extremely rare < 50 years old
– Pooled analysis 1435 pt, only 2 < 50yo
Temporal artery findings (large, absent pulse,
tenderness) fairly specific but not sensitive
Normal ESR (< 20 mm/hr) excludes dx, moderate ESRs
don’t (20-50 mm/hr)
– <20 mm/hr
– <40 mm/hr
– < 50 mm/hr
96% sensitive
95% sensitive
89% sensitive
Giant Cell Arteritis: some pearls
Temporal artery biopsy
– Initial bilateral biopsies 88% sensitive
– Repeat if initial biopsies negative
– Biopsy will be abnormal for weeks after initiation of steriod;
try to have it done soon but not emergently
– Prednisone 60 mg po od
– START before biopsy
Headache is a high risk complaint.
Consider serious causes in every
Majority of badness excluded with
good history and physical.
More complex than just ordering CT
Headache and normal CT head;
ddx of “bad” causes?
Ischemic stroke
HTN encephalopathy
CO toxicity
CNS infection
Carotid/vertebral dissection
Which can be excluded
By hx/pe?
Headache and normal CT head;
ddx of “bad” causes?
Ischemic stroke - hx and physical
HTN encephalopathy - physical
Pre-eclampsia - hx and physical
CO toxicity - hx
Vasculitis/GCA - hx
AACG - physical
Which can be excluded
By a normal LP?
CNS infection
Carotid/vertebral dissection - CTA/MRA
Headache and normal CT head;
ddx of “bad” causes?
Ischemic stroke - hx and physical
HTN encephalopathy - physical
CO toxicity - hx
Vasculitis/GCA - hx
AACG - physical
CNS infection --------------> LP
CVT -------------------------> LP (+/- CTV)
IIHTN -----------------------> LP
SAH -------------------------> LP
Carotid/vertebral dissection - CTA/MRA/Angio
Lumbar puncture is a
test to exclude some
causes of headache
Opening pressure is worthwhile.
Approach to ED headache
History and Physical
Review DDx and serious causes
Diagnosis identified
Benign cause
Concern for
serious cause
Plain CT head
Lumbar Puncture
Headache motherhood
Chronic migrainers with toradol allergies get badness
to. Be diligent.
Approach headache like chest pain - good hx/pe and
directed investigations to exclude badness.
Have a ddx of badness and “run the list” with every
Headache is more than migraine and SAH.
Anyone can thing to order a CT head. A good
clinician will pick up the less common but serious
Older patient with no hx migraine: be cautious.
Miscellaneous pearls
What INR before LP?
 What platelet level is c/I to LP?
 35yo healthy male, collapsed, Vfib arrest,
bystander cpr and defib at 5min, persistent
coma, diagnosis?
 How to decrease post LP headache?
– Needle size, pokes, non-cutting, stylet
– Bedrest and IVF not helpful

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